Senescence and apoptosis: dueling or complementary cell fates?
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- Bennett G Childs
- Departments of Biochemistry and Molecular Biology Mayo Clinic Rochester MN USA
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- Darren J Baker
- Pediatric and Adolescent Medicine Mayo Clinic Rochester MN USA
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- James L Kirkland
- Robert and Arlene Kogod Center on Aging Mayo Clinic Rochester MN USA
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- Judith Campisi
- Buck Institute for Research on Aging Novato CA USA
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- Jan M van Deursen
- Departments of Biochemistry and Molecular Biology Mayo Clinic Rochester MN USA
説明
<jats:title>Abstract</jats:title><jats:p>In response to a variety of stresses, mammalian cells undergo a persistent proliferative arrest known as cellular senescence. Many senescence‐inducing stressors are potentially oncogenic, strengthening the notion that senescence evolved alongside apoptosis to suppress tumorigenesis. In contrast to apoptosis, senescent cells are stably viable and have the potential to influence neighboring cells through secreted soluble factors, which are collectively known as the senescence‐associated secretory phenotype (<jats:styled-content style="fixed-case">SASP</jats:styled-content>). However, the <jats:styled-content style="fixed-case">SASP</jats:styled-content> has been associated with structural and functional tissue and organ deterioration and may even have tumor‐promoting effects, raising the interesting evolutionary question of why apoptosis failed to outcompete senescence as a superior cell fate option. Here, we discuss the advantages that the senescence program may have over apoptosis as a tumor protective mechanism, as well as non‐neoplastic functions that may have contributed to its evolution. We also review emerging evidence for the idea that senescent cells are present transiently early in life and are largely beneficial for development, regeneration and homeostasis, and only in advanced age do senescent cells accumulate to an organism's detriment.</jats:p>
収録刊行物
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- EMBO reports
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EMBO reports 15 (11), 1139-1153, 2014-10-13
Springer Science and Business Media LLC
